Apnea of infancy (AOI) and subsequent siblings of SIDS victims (SS- SIDS) have abnormalities in control of sleep and breathing which may be important in sudden infant death syndrome (SIDS). A normal defense mechanism which terminates apnea during sleep is arousal. A majority of AOI and SS-SIDS infants have an abnormal hypoxic arousal response (HAR). This abnormal defense mechanism may prevent the infant from terminating a hypoxic event, or apnea, during sleep. Two hypotheses for the abnormal HAR are the focus of this research. Hypothesis 1: The abnormal HAR in AOI and SS-SIDS is due to a test this, control, AOI, and SS-SIDS infants, 30-50 per group, and 1-6 months, will be studied. HAR will be tested by having the infant breathe P1O2 80 mm Hg until arousal or for 3 minutes. Arousal responses to sensory stimuli (sound, light) will be tested by randomly presenting computer generate burst of white noise and light flashes to the sleeping infants. Arousal to temperature will be tested by having infants sleep on a cooling blanket while changing the temperature 5 C above and below thermal neutrality. Sleep records will be scored for sleep and respiratory events by technicians blinded to the pattern of stimuli. Events and stimuli will be correlated. If the abnormal HAR in AOI and SS-SIDS is due to a generalized arousal deficit, infants with abnormal HAR should have decreased arousal to sensory stimuli. Hypothesis 2: The abnormal HAR in AOI and SS-SIDS is due to habituation to chronic episodic hypoxia. To study this, the above infants will have continuous recordings of respirations, ECG, and arterial oxygen saturation (SaO2) by pulse oximetry performed overnight, fo. 3 nights. Time with SaO2 less that 95%, 90%,80%, and 70% will be calculated. Recordings will be repeated during an upper respiratory infection. If the abnormal HAR is due to habituation, then infants with an abnormal HAR should have more frequent or severe dasaturations than those with normal HAR or than controls.